The role of complement and CD4 T cells in preeclampsia and offspring neurodevelopment
Preeclampsia is a multifactorial hypertensive disorder of pregnancy. Dysregulated innate complement activity and skewing of adaptive CD4+ T helper (T<sub>H</sub>) responses (↑T<sub>H</sub>1/T<sub>H</sub>17, ↓Treg) contribute to maternal hypertension, endothelial dysfunction, and proteinuria. Children exposed <i>in utero</i> to preeclampsia have higher rates of neurodevelopmental disorders. Because complement and T<sub>H</sub> pathways also shape normal neurodevelopment, converging clinical and experimental data link preeclampsia to immune dysregulation at the maternal-fetal interface, increased fetal exposure to inflammatory signals, and altered fetal brain development with downstream neurobehavioral effects. Interactions between complement (e.g., C3a/C5a) and T<sub>H</sub> cells is a plausible driver of these effects, but the precise mechanisms, timing, and tissue compartments remain to be defined.
Authors
- Jean F. Regal (ORCID: https://orcid.org/0000-0001-5713-0891)
- Sabrina M. Scroggins
- Courtney A. O’Kane
Institutions
- University of Minnesota, Duluth (US)
Publication Details
- Journal
- Current Opinion in Physiology
- Published
- 2026-02-13
- DOI
- https://doi.org/10.1016/j.cophys.2026.100927
- Primary Topic
- Pregnancy and preeclampsia studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00